Biochemical and morphological changes observed in rat muscles following consumption of excessive L-tryptophan and atherogenic diets.
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Acid Phosphatase↗
Biomedical subjects
E Livne
Publications and source records attributed to E Livne.
Testicular neovascularization by "omentotesticulopexy': a possible adjuvant in the surgical correction of high undescended testes.
The surgical repair of "very high" undescended testes may bring about testicular atrophy, as a result of impaired vascular supply, whether caused unintentionally by extensive dissection, or deliberately when the Fowler-Stephens operation is employed. In this experimental study, improvement of the vascular supply by means of "omentotesticulopexy" (an omental flap pexied to the rat testis) before or concomitant with spermatic vessel division (known as the Fowler-Stephens operation) was achieved and demonstrated by angiographic studies. The authors believe that the addition of "omentotesticulopexy" to the Fowler-Stephens operation will reduce the rate of testicular atrophy among patients with high undescended testes.
Angiography↗
Osteosarcomagenic doses of radium (224Ra) and infectious endogenous retroviruses enhance proliferation and osteogenic differentiation of skeletal tissue differentiating in vitro.
Cartilage tissue from embryonic mice which undergoes osteogenic differentiation during in vitro cultivation was used to study the effect of osteosarcomagenic doses of alpha-irradiation and bone-tumor-inducing retroviruses on proliferation and phenotypic differentiation of skeletal cells in a defined tissue culture model. Irradiated mandibular condyles showed dose-dependent enhancement of cell proliferation at day 7 of the culture and increased osteogenic differentiation at day 14. Maximal effects were found with 7.4 Bq/ml of 224Ra-labeled medium. Doses of 740 and 7400 Bq/ml of 224Ra-labeled medium induced increasing cell death. Retrovirus infection enhanced osteogenic differentiation and extended the viability of irradiated cells. After transplantation none of the treated tissues developed tumors in syngeneic mice.
Animals↗
Matrix synthesis in mandibular condylar cartilage of aging mice.
Osteoarthritic (OA) lesions often develop along the articular surface of mandibular condylar cartilage of aging mice. Metabolic activities of chondrocytes in condylar cartilage of newborn to 18-month-old mice were evaluated morphologically and biochemically in vivo and in vitro. In the period between birth and 3 months of age, marked age-dependent reductions in the number of cells per unit area (-56.43%), in DNA (-64.38%) and in glycosaminoglycan (GAG) (-46.32%) contents were observed. In the same time period, protein content remained almost constant. Reduced rates in the incorporation of [3H]thymidine, [3H]leucine and [35S]sulfate between birth and 3 months of age (-81.60%, -25.98% and -67.75%, respectively) were also observed in vitro. Collagen synthesis was similarly reduced, from 38.70% in newborns to 27.86% in 18-month-old animals. Morphology and autoradiography in mandibular cartilage revealed that the reductions of cellularity and of sulfated macromolecular synthesis appeared to be more pronounced along the articular surface. In this region OA lesions were often observed. It may thus be that the combination of reduced sulfated GAGs and the decreased number of cells in this region could result in tissue with architecture that is less suited to withstanding stress and thus more prone to the development of the typical OA lesions that are seen along the articular surfaces of mandibular cartilage in aged mice.
Aging↗
Typical and atypical neuroleptics induce alteration in blood-brain barrier and brain 59FeCl3 uptake.
Long-term neuroleptic medication of schizophrenic patients induces extrapyramidal motor side effects, of which tardive dyskinesia (TD) is the most severe. The etiology of TD is still obscure. Recently, it was suggested that abnormal iron metabolism may play a crucial role in neuroleptic-induced dopamine D2 receptor super-sensitivity. The apparent relationship between neuroleptics and iron is further supported by the increase of iron in the basal ganglia of patients with TD. We now report on the ability of neuroleptic to alter the blood-brain barrier in the rat and to potentiate the normally limited iron transport into the brain. Thus, chronic treatment of rats with chlorpromazine and haloperidol facilitated 59Fe3+ uptake into brain cells. In contrast, clozapine, an atypical antipsychotic neuroleptic with little extrapyramidal motor side effects, caused iron sedimentation in brain blood vessels with no sign of detectable iron in the cells. Moreover, chronic treatment with chlorpromazine and haloperidol caused a 43% and 24% reduction, respectively, in liver nonheme iron, whereas clozapine induced an 81% increase. The apparent different potentials of chlorpromazine, haloperidol, and clozapine to increase iron transport into the brain from its peripheral stores may be linked to the severity of extrapyramidal motor side effects they induce and to the pathophysiology of TD.
Animals↗
In vitro response of articular cartilage from mature mice to human transforming growth factor beta.
The ability of human transforming growth factor-beta 1 (hTGF-beta 1) to induce proliferation and matrix synthesis in articular cartilage of aging mice was studied using an organ culture system of mandibular condylar cartilage. An increased incorporation of 3H-thymidine into DNA and of 35S-SO4 into sulfated glycosaminoglycans was observed in cultures supplemented with 1-10 ng/ml TGF-beta and with 1% fetal calf serum. In these cultures numerous clusters of chondrocytes containing a well-developed rough endoplasmic reticulum were seen. Articular cartilage from mature animals often develops osteoarthritic degenerative lesions, thus the induction of cell proliferation and of matrix synthesis may be an indication of a tissue repair process in cartilage from maturing animals.
Aging↗
In vitro effect of hormones and growth factors on the incorporation of [3H]leucine, [35S]sulfate and [3H]proline by chondrocytes of aging mice.
The ability of parathyroid hormone (PTH 1-84), dexamethasone, prostaglandin E1 (PGE1), prostaglandin E2 (PGE2) and human transforming growth factor beta (hTGF-beta) to stimulate the synthesis of matrical components in articular cartilage of aging mice, was studied in an organ culture system. A marked age-dependent decrease was observed in the synthesis of sulfated glycosaminoglycans (GAGs), protein, collagen digestible protein (CDP) and non-collagen protein (NCP) between 1 and 18 months of age. The addition of hTGF-beta (1 ng/ml) into the culture medium resulted in a significant (P < 0.01) increase of both protein and sulfated GAGs in condylar cartilage from animals aged 1, 3, 6 and 12 months. PGE2 (10 micrograms/ml) induced [3H]leucine and [35S]SO4 incorporation into condylar cartilage from 1, 3 and 6 months old animals. A stimulatory effect of PGE1 (10 micrograms/ml) on [3H]leucine incorporation was noted at 1 and 3 months of age. The effect of PTH appeared to be stimulatory only for protein synthesis in young (1 and 3 months old) animals, whereas it had no effect at 6, 12 and 18 months of age. In contrast, dexamethasone exerted a stimulatory effect on young adults (6 months old) and in matured (12 months old) animals, respectively and a slight inhibitory effect on young (1 and 3 months old) animals. [3H]Proline incorporation was enhanced by all the factors tested in 1-month-old animals. In cultures from 6- and 18-month-old animals only PGE1 and PGE2 appeared to be stimulatory. It is concluded that synthesis of protein, sulfated GAGs and collagen by chondrocytes from maturing and osteoarthritic senescent animals can be stimulated by hormones and growth factors. The efficiency of this response, however, varied according to the animal's age and the factor studied.
Aging↗
Diarthroses in the mouse: from different cellular structure to similar joint appearance.
The structure and function of two major joints, the humeroscapular and the squamoso-mandibular joints in mice, are compared. The specific roles that these two joints fulfill during early postnatal period are reflected in a different cellular organization observed in them. Following maturation, when similar functional needs are stressed upon these two joints, similar homologous structures are detected in both of them. A possible conceptual explanation for these observations and their relatedness to the human equivalent joints are discussed.
Animals↗
Effect of growth hormone on gastrocnemius muscle of aged rats after immobilization: biochemistry and morphology.
Immobilization of limbs of aged animals is associated with swift muscular damage and atrophy. We investigated the effect of rat growth hormone (rGH) on immobilized hindlimb muscles of 26-mo-old rats. Administration of rGH significantly reduced muscle weight loss and muscle protein oxidation caused by immobilization. Capillary blood volume, measured by photoplethysmography of the hindlimb, showed a 34% reduction in immobilized animals, which was eliminated by rGH. The activity of creatine phosphokinase in immobilized gastrocnemius muscle was significantly reduced by immobilization. This damage was diminished by rGH administration. Similarly, the increase in acid phosphatase activity in immobilized muscle was reduced after rGH treatment. Morphologically, marked muscle atrophy and fiber disorientation were observed in immobilized limbs. Therapy with rGH prevented some of these changes. These results indicate that administration of rGH may provide a useful means to attenuate the degenerative effects of limb immobilization of aged rats, as evident from physiological, biochemical, and morphological parameters.
Acid Phosphatase↗
Iron modulates neuroleptic-induced effects related to the dopaminergic system.
Long-term neuroleptic medication to schizophrenic patients is often associated with extrapyramidal side effects, of which tardive dyskinesia is the most severe. The mechanism by which neuroleptics induce these side effects is unclear. The dopaminergic system is the main target with which the neuroleptics interact in the brain. Intact dopaminergic function is dependent on normal iron metabolism. Thus, the relationship between iron and the neuroleptics may elucidate some new aspects of their mechanism of action. Indeed, peripheral iron status plays a crucial role in neuroleptic-induced dopamine supersensitivity. Moreover, neuroleptics such as haloperidol and chlorpromazine, alter the blood brain barrier (BBB) of the rat and enhance the normally restricted iron transport into the brain. Increased brain iron levels may be related to the toxic effects of these drugs since clozapine, an atypical neuroleptic with a low incidence of extrapyramidal side effects, prohibits iron uptake into the brain but causes sedimentation of iron in brain blood vessels. The demonstration that peripheral iron concentrations affect neuroleptic-induced dopamine receptor supersensitivity as well as iron transport into the brain may have therapeutic significance. In addition, the different potentials of typical and atypical neuroleptics to increase iron transport into the brain may be related to the severity of the side effects they induce and to the pathophysiology of tardive dyskinesia.
Animals↗
Tibia development in turkeys and chickens as affected by early-age feed restriction.
Tibia development was studied by histomorphometry in male chickens and turkeys fed ad libitum throughout the growing period, or subjected to an early-age (1-week) severe feed restriction for 6 and 14 days, respectively. In turkeys, the rates of longitudinal bone growth and epiphyseal width growth, both dependent on the activity of chondrocytes, proceeded rapidly and reached maxima at early ages of 24 and 11 days, respectively. Moreover, longitudinal bone growth and the growth of epiphyseal width were reduced during early-age feed restriction, in both chickens and turkeys. On the other hand, the rate of growth of metaphyseal width, determined by activity of bone cells such as osteoclasts and osteoblasts, reached in turkeys a maximum at the relatively late age of 70 days, and was not influenced by feed restriction. Rhythmic variation characterized the temporal behavior of the height of the hypertrophic and non-hypertrophic zones of the growth plate, the trabecular width, and the osteoclasts number at the subchondral region. Rhythmicity appeared similar in both ad libitum-fed and early-age feed-restricted birds of both species. The height of the non-hypertrophic epiphyseal cartilage appeared not to change, whereas the hypertrophic zone decreased with age and early-age feed restriction, demonstrating the importance of cartilage cell hypertrophy as a main determinant of longitudinal bone growth. Sexual maturation was accompanied by the disappearance of both hypertrophic and non-hypertrophic zones of the epiphyseal growth plate and the end of bone elongation. Trabecular width at the end of bone elongation. Trabecular width at the subchondral region increased while osteoclast number decreased with age, reflecting the net increase in bone mass, but were not affected significantly by early age feed restriction. Compensatory growth of the early-age feed-restricted birds, resulted in the complete recovery of affected bone variables within a few weeks of resumed ad libitum feed intake.
Aging↗
Activity of alkaline phosphatase in rat skeletal muscle localized along the sarcolemma and endothelial cell membranes.
Alkaline phosphatase (AP), a membrane-associated glycoprotein which enhances the hydrolysis of monophosphate esters at alkaline pH, is widely distributed in animal tissues. AP activity is increased in a variety of muscle disorders, i.e., myopathies and denervation. Established histochemical methods at the light microscopy level failed to demonstrate AP in skeletal muscles. In the present study we applied the Gomori lead nitrate method for ultrastructural examination of AP in rat gastrocnemius muscles and showed that the enzyme was linked to the sarcolemma of the striated muscle and to the membranes of endothelial cells in adjacent capillaries. In comparison with ATPase activity, AP activity was inhibited by both levamisole and a pH of 7.2, but not by ouabain. Hence, it appears that in skeletal muscles AP is active at a high pH and is bound to cell membranes.
Alkaline Phosphatase↗
The assay of soluble IL-2R receptor levels in graft microenvironment can be helpful in differential diagnosis of transplant dysfunction.
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Biomarkers↗
Growth and differentiation of murine cartilage cells in vitro following a short-term exposure to triamcinolone acetonide.
Measurements of 3H-thymidine incorporation, quantitative autoradiography and morphometry were used to evaluate cell behavior during the recovery of mandibular condylar cartilage cultures following short-term exposure to a corticosteroid hormone in vitro. Apical segments of mandibular condyles of newborn mice were initially incubated in the presence of the hormone triamcinolone acetonide (10(-6) M) for 24 h and were thereafter cultured for additional 6 days in hormone-free medium. The present results indicated that the treatment led to a decrease in the rate of incorporation of 3H-thymidine, a feature that lasted for 48 h following the removal of the hormone. Quantitative 3H-thymidine autoradiography of explants that were labeled in the presence of the hormone further substantiated the initial suppressive effect of the hormone on cellular proliferation, a feature that was followed by a recovery. Differences were noted in the pattern of distribution of labeled cells: in control explants, labeled cells progressively moved from the chondroprogenitor compartment into the differentiated portion of the cartilage; in hormone-treated explants, 3H-thymidine labeled cells were confined to the progenitor layer up to 5 days after the treatment and only then appeared in the chondrocytic compartment. The hormone's adverse effect upon differentiation was manifested by both morphology, and by causing a significant increase in the size of the progenitor layer (up to 50.5% on 4th post-treatment day) along with a 70.5% reduction in the size of chondroblastic layer. We conclude that a short-term exposure to a glucocorticoid hormone in vitro interferes with proliferation of chondroprogenitor cells and their subsequent differentiative pathway.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Histochemical study of matrical components in the mandibular condyle of the neonatal mouse.
In the mandibular condyle of the newborn mouse the chondroprogenitor (CP) zone is the only layer that incorporates 3H-thymidine thus serving the source for cells of the cartilage lineage. Ultrastructurally these cells have a mesenchymal appearance surrounded by collagen fibrils as well as by additional filaments that become apparent following fixation with ferrocyanide-reduced OsO4. In addition, electron-dense particles indicative of proteoglycans are scattered throughout the matrix in the CP zone as well as in the chondroblastic and hypertrophic zones. Following labeling with 35S-sulfate the CP zone as well as the other compartments revealed a substantial number of grains following processing for autoradiography. The number of grains per cell was highest in the hypertrophic zone. Indirect immunofluorescence indicated the presence of fibronectin in the articular surface, CP zone and in the hypertrophic zone. The immunogold method localized fibronectin intracellularly in CP cells and extracellularly in the hypertrophic zone. Therefore, in the mandibular condyle the CP cells which are capable for DNA synthesis are also involved in the synthesis of macromolecules of which some are specific for the cartilage phenotype, while others are associated with other functions of connective tissue cells.
Animals↗
Changes in growth patterns in mouse condylar cartilage associated with skeletal maturation and senescence.
The squamoso-mandibular joint (SMJ) represents one of the most active joints in the mouse. In the young animal the main function of condylar cartilage in the SMJ is to serve as a growth center for the developing mandible. This first phase of skeletal growth lasts up to the age of 6-8 weeks, and is manifested by appositional growth of cartilage followed by endochondral ossification. Thereafter, the condylar cartilage gradually changes its function and serves mainly as an articulating surface for the joint. Consequently, the cartilage changes from a calcifying hyaline cartilage to a fibrous non-calcifying cartilage. The latter phase lasts through the stage of maturation (6 months of age) and it is manifested by a combination of appositional and interstitial patterns of cellular growth. Thereafter, the third phase develops which is characterized by degenerative changes that typify the aging process. In vivo autoradiography with [3H]-thymidine indicated that in the very young animal labeled cells are confined to the chondroprogenitor (proliferative) zone of the condylar cartilage. With maturation, the dimension of this zone as well as the number of labeled cells decrease, so that by 3 months of age the labeling index decreases by 30%. By the age of 6, 12 and 18 months, almost no cells take up the radioisotope while the total number of cells declines. During senescence only a very limited interstitial growth is taking place, a feature that might be associated with the repair processes that accompany the onset of osteoarthritic lesions.
Aging↗
The mouse mandibular condyle: an investigative model in developmental biology.
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Animals↗
Articular chondrocytes lose their proliferative activity with aging yet can be restimulated by PTH-(1-84), PGE1, and dexamethasone.
Mouse mandibular condyles develop spontaneous degenerative changes by 6 months of age, hence providing a good in vivo model for studies related to processes associated with the onset and progression of age-related osteoarthritis. Further, this joint provides an appropriate system to investigate the potential of articular cartilage to respond to hormones and local growth factors in old age. The present study examined (1) the age-related changes in [3H]thymidine incorporation by articular chondrocytes in the mouse mandibular condyle, and (2) the effect of systemic and local factors upon the tissue's ability to resume DNA synthesis. Condyles of female CW-1 mice ranging from 3 to 18 months of age were cultured in the presence of PTH-(1-84) (2 micrograms/ml), PGE1 (20 micrograms/ml), dexamethasone (10(-7) M), and MSA (5 micrograms/ml) and were concomitantly labeled with [3H]thymidine. Autoradiographs were analyzed quantitatively and revealed (1) a significant (p less than 0.01) age-related decrease (-80%) in the labeling index of the articular cartilage, and (2) the ability of old tissues to resume DNA synthesis following in vitro treatment with PTH-(1-84), PGE1, and dexamethasone. Concomitant quantitative incorporation studies further substantiated the autoradiographic findings. Hence, these factors possess a direct stimulatory effect upon senescent chondrocytes involved in an advanced stage of spontaneous osteoarthritis.
Aging↗